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Brian W. J. Mahy
Researcher at University of Cambridge
Publications - 31
Citations - 2160
Brian W. J. Mahy is an academic researcher from University of Cambridge. The author has contributed to research in topics: Virus & RNA. The author has an hindex of 19, co-authored 30 publications receiving 2044 citations. Previous affiliations of Brian W. J. Mahy include University of California, San Francisco & Rockefeller University.
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The virion glycoproteins of Ebola viruses are encoded in two reading frames and are expressed through transcriptional editing.
TL;DR: Phylogenetic analysis indicates that EBO virus subtypes are genetically diverse and that the recent Ivory Coast isolate represents a new (fourth) subtype of EBO Virus, and is virtually identical to the virus that caused a similar epidemic in Yambuku, Zaire almost 20 years earlier.
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The synthesis of Sendai virus polypeptides in infected cells
Robert A. Lamb,Robert A. Lamb,Brian W. J. Mahy,Brian W. J. Mahy,Purnell W. Choppin,Purnell W. Choppin +5 more
TL;DR: The results of pulse and pulse-chase experiments suggest that large, polyprotein precursors are not involved in Sendai virus replication, and that polypeptides are synthesized from monocistronic messenger RNA species.
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Polypeptides specified by the influenza virus genome: I. Evidence for eight distinct gene products specified by fowl plague virus
TL;DR: The structural polypeptides of fowl plague virus (influenza A) and those synthesized in fowl Plague virus-infected chick embryo fibroblasts have been analyzed by high resolution polyacrylamide gel electrophoresis and shown to be distinct by tryptic peptide mapping.
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Ethidium bromide inhibits appearance of closed circular viral DNA and integration of virus-specific DNA in duck cells infected by avian sarcoma virus.
TL;DR: Ethidium bromide reduces the formation of superhelical viral DNA and concurrently blocks integration of the viral genome, which results in the inhibition of virus replication.
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Transcription and replication of influenza virus RNA.
TL;DR: Analysis of A(−) cRNA and vRNA accumulations in infected cells showed that the A(+) c RNA synthesis precedes vRNA synthesis and net accumulation of A- cRNA ceased by 3 hr postinfection (pi), and significant amounts of vRNA in excess of input vRNA were detected by about 2 hr pi and continued to accumulate in both nucleus and cytoplasm at least up to 6 hr pi.